HIV-1 (人免疫缺陷病毒-1)感染不能将干扰素导入其所感染的细胞中，但其中所涉及的机制却没有被确定。树突细胞（皮肤、粘膜和淋巴组织中的免疫细胞）调控病原体的先天检测及在适应性免疫中所涉及的其他免疫细胞的激活，但却不是为了对付HIV。树突细胞对HIV感染是有抵抗力的，虽然它们也的确与该病毒结合，并且被认为帮助T-helper细胞的感染。
现在研究表明，当HIV感染的通常阻断被树突细胞绕过时（通过暴露于 Vpx accessory 来实现，它是一种来自猴免疫缺陷病毒SIVmac的蛋白），HIV便不会诱导I-型干扰素响应和T-细胞激发。HIV-1的毒性也许与其能够通过呆在树突细胞之外来逃避先天免疫的能力有关，而且这一策略的运用可能有助于疫苗设计。（生物谷Bioon.com）
生物谷推荐英文摘要：
Nature doi:10.1038/nature09337
A cryptic sensor for HIV-1 activates antiviral innate immunity in dendritic cells
Nicolas Manel,Brandon Hogstad,Yaming Wang,David E. Levy,Derya Unutmaz& Dan R. Littmandan.littman
Dendritic cells serve a key function in host defence, linking innate detection of microbes to activation of pathogen-specific adaptive immune responses1, 2. Whether there is cell-intrinsic recognition of human immunodeficiency virus (HIV) by host innate pattern-recognition receptors and subsequent coupling to antiviral T-cell responses is not yet known3. Dendritic cells are largely resistant to infection with HIV-14, but facilitate infection of co-cultured T-helper cells through a process of trans-enhancement5, 6. Here we show that, when dendritic cell resistance to infection is circumvented7, 8, HIV-1 induces dendritic cell maturation, an antiviral type I interferon response and activation of T cells. This innate response is dependent on the interaction of newly synthesized HIV-1 capsid with cellular cyclophilin A (CYPA) and the subsequent activation of the transcription factor IRF3. Because the peptidylprolyl isomerase CYPA also interacts with HIV-1 capsid to promote infectivity, our results indicate that capsid conformation has evolved under opposing selective pressures for infectivity versus furtiveness. Thus, a cell-intrinsic sensor for HIV-1 exists in dendritic cells and mediates an antiviral immune response, but it is not typically engaged owing to the absence of dendritic cell infection. The virulence of HIV-1 may be related to evasion of this response, the manipulation of which may be necessary to generate an effective HIV-1 vaccine.
